Four diets were formulated to contain: 16% protein and 0.4% phosphorus-diet 1; 16% protein and 1.4% phosphorus-diet 2; 32% protein and 0.4% phosphorus-diet 3; and 32% protein and 1.4% phosphorus-diet 4. Forty-eight dogs were fed diet 1 for 3 months after surgical reduction of renal mass, then were allotted to 4 groups of 12 dogs each, with equal mean values for glomerular filtration rate (GFR). Dog of groups 1-4 were fed diets 1-4, respectively, for 24 months. Data collected from the dogs during and at termination of the study were analyzed statistically for effects of dietary protein, phosphorus (P), time, and interactions between these factors. During the 24 months of study, 24 dogs developed uremia and were euthanatized for necropsy. Necropsy also was performed on the remaining 24 dogs after they were euthanatized at the end of the study. Dog survival was significantly enhanced by 0.4% P diets (vs 1.4% P diets), but survival was not significantly influenced by amount of dietary protein. The 0.4% P diets (vs 1.4% P diets) significantly increased the period that GFR remained stable before it decreased, but dietary protein did not have significant effect. Significant blood biochemical changes attributed to P, protein, and time were identified during the study. Terminally, plasma parathyroid hormone concentration was significantly increased from prediet values in all groups of dogs. Urine protein excretion was not significantly affected by dietary amount of either protein or P, when measured by either timed urine collection or urine protein-to-creatinine ratio. A tendency was seen for increased protein excretion with passage of time. Histologic and mineral analyses of kidneys removed at necropsy revealed some significant difference attributable to diet, but differences were more marked when diet was ignored, and the 24 surviving dogs were compared with the 24 that developed uremia. Overall, amount of dietary P was more important than amount of dietary protein for preventing adverse responses. However, because renal damage specifically attributable to either dietary component was not obvious, it is possible that the effects of P were manifested by extrarenal mechanisms.

Serum lipoprotein concentrations, routine serum biochemical values, and morphologic changes of the liver were evaluated in cats undergoing weight loss. Food was withheld from 6 obese and 6 control cats for 3 days (days 0 to 2), followed by feeding 50% of previous food intake for 26 days (days 3 to 28). Percutaneous liver biopsy specimens were obtained from all cats on days 0, 7, 14, and 28. Blood samples for serum biochemical analysis and lipoprotein profiles were obtained on days 0, 3, 7, 14, and 28. All cats lost weight throughout the study, and none developed signs of chemical illness, including those of idiopathic hepatic lipidosis syndrome. Serum total cholesterol concentrations decreased initially in all cats, but rapidly returned to normal after day 3 in obese cats, suggesting altered cholesterol metabolism during dietary restriction. Low-density lipoprotein concentrations decreased throughout the study in control cats, but were unchanged in obese cats. Examination of liver biopsy specimens from each cat revealed minimal lipid accumulation in all specimens, although some specimens contained hydropic degeneration.

Amino acid profiles and serum albumin and serum total protein concentrations were evaluated in dogs with renal disease. Nine dogs ranging in age from 1 to 15 years were identified as having mild to moderate chronic renal failure (CRF; exogenous creatinine clearance, 0.5 to 2.13 ml/kg of body weight/min). These dogs and a group of 10 clinically normal control dogs were fed a diet containing 31% protein for 8 weeks, at which time serum and urine amino acid assays and clearance studies were performed. All dogs then were fed a diet containing 16% protein for 8 weeks and then reevaluated. Chronic renal failure was associated with mild abnormalities in serum concentrations of amino acids. When fed the higher protein diet, dogs with CRF had lower serum concentrations of glutamine, leucine, proline, and serine and higher serum concentrations of cystathionine and 3-methylhistidine than clinically normal control dogs. When fed the low protein diet, dogs with CRF had lower serum serine concentrations and higher serum concentrations of cystathionine, phenylalanine, and 3-methylhistidine. Urine excretion of amino acids in all dogs on both diets was low, and dogs with CRF had lower renal clearances of 3-methylhistidine than control dogs. There were no significant differences in concentrations of serum albumin and total solids between either group, regardless of diet. We concluded that dogs with mild to moderately severe CRF have mild abnormalities of serum free amino acid concentrations, but renal conservation of essential amino acids is not impaired.

Exogenous creatinine clearance, urinary electrolyte excretions, calcium and phosphorus balance, serum cholesterol concentration, arterial blood pressure, and body weight were evaluated in dogs with chronic renal failure that were fed 2 commercial diets. Nine dogs ranging in age from 1 to 15 years were identified as having mild to moderate chronic renal failure (CRF, exogenous creatinine clearance = 0.5 to 2.13 ml/kg of body weight/min). These dogs and a group of 10 clinically normal controls were fed a diet containing 31% protein for 8 weeks at which time hematologic and biochemical evaluations and clearance studies were performed. All dogs then were fed a phosphorus-restricted diet containing 16% protein and then reevaluated after 8 weeks. The dogs in this study had hematologic and biochemical abnormalities typical of CRF. Urine absolute and fractional excretion of electrolytes was higher in dogs with CRF than in controls and was affected by diet. Serum cholesterol concentration was higher in dogs with CRF and increased in those dogs after feeding the low protein diet. Changes in dietary sodium intake did not affect arterial blood pressure. The phosphorus-restricted diet did not affect serum amino terminal parathyroid hormone concentration in either group. Control dogs lost body weight, whereas dogs with CRF gained weight when fed the low protein diet. We concluded that dogs with mild to moderately severe CRF have the same biochemical abnormalities and response to dietary restriction of protein and phosphorus as has been previously reported in dogs with experimentally induced CRF. Restriction of dietary sodium may not decrease arterial blood pressure in some dogs with CRF. Dogs with CRF may be predisposed to hypercholesterolemia when fed restricted protein commercial diets, and reduction of dietary phosphorus intake may be inadequate to control renal secondary hyperparathyroidism in dogs with CRF.

Twenty-four dogs with induced, severe chronic renal failure were allotted to 2 groups of 12 each. Group-A dogs were fed a 0.4% phosphorus (P)/0.6% calcium, 32% protein diet, and group-B dogs were fed a 1.4% P/1.9% calcium, 32% protein diet. Dogs were studied over 24 months to determine clinical status, survival, blood biochemical alterations, glomerular filtration rate (GFR), urinary excretion of P and protein, renal morphologic changes, and renal tissue concentrations of calcium, P, and magnesium. Group-A dogs developed statistically significant differences from group-B dogs in several blood biochemical values (PCV and total solids, calcium, P, potassium, sodium, chloride, total CO2 (TCO2), anion gap, and parathyroid hormone concentrations) and in urinary P excretion. Mean (+/- SEM) GFR values in group-A and group-B dogs were nearly identical when diets were initiated (group A = 0.73 +/- 0.05 ml/min/kg of body weight; group B = 0.72 +/- 0.08 ml/min/kg), but significantly (P = 0.0346) lower GFR developed in group-B than in group-A dogs over time. At 24 months, GFR in survivors was 0.83 +/- 0.08 and 0.63 +/- 0.15 ml/min/kg for dogs of groups A and B, respectively. Other measurements favored the hypothesis that P/calcium restriction was beneficial, but values failed to reach statistical significance. Survival was greater at 24 months in group-A than in group-B (7 vs 5) dogs, and renal tissue concentrations of calcium and P were higher in group-B than in group-A dogs. Differences were not detected between groups in urinary excretion of protein and in the type or severity of renal lesions. We conclude that P/calcium restriction at 32% protein intake is beneficial to dogs with chronic renal failure, but that the degree of restriction imposed in group-A dogs of this study did not prevent development of abnormalities. Factors other than dietary P/calcium intake may have a role in progression of renal failure to uremia.